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Jena, Germany

Costa A.C.B.P.,Sao Paulo State University | Costa A.C.B.P.,Hans Knoell institute | Pereira C.A.,Sao Paulo State University | Freire F.,Sao Paulo State University | And 2 more authors.
Mycoses | Year: 2013

Biofilm formation is one of the most important attributes for virulence in Candida species and contributes to increased resistance to antifungal drugs and host immune mechanisms. These features have led to the development of several methodologies to reproduce a sessile community in vitro that can be used to study the development of a biofilm, its interaction with other microorganisms and the environment, and its susceptibility to available antifungal agents and also to search for new therapy strategies. The purpose of this review is to describe the most commonly used methods to study Candida biofilms in vitro, to discuss the benefits and limitations of the different methods to induce biofilm formation, and to analyse the architecture, viability and growth kinetics of Candida biofilms. © 2013 Blackwell Verlag GmbH. Source

Duggan S.,Leibniz Institute for Natural Product Research and Infection Biology | Leonhardt I.,Leibniz Institute for Natural Product Research and Infection Biology | Hunniger K.,Leibniz Institute for Natural Product Research and Infection Biology | Kurzai O.,Leibniz Institute for Natural Product Research and Infection Biology | And 2 more authors.
Virulence | Year: 2015

Candida albicans is a major cause of bloodstream infection which may present as sepsis and septic shock - major causes of morbidity and mortality world-wide. After invasion of the pathogen, innate mechanisms govern the early response. Here, we outline the models used to study these mechanisms and summarize our current understanding of innate immune responses during Candida bloodstream infection. This includes protective immunity as well as harmful responses resulting in Candida induced sepsis. Neutrophilic granulocytes are considered principal effector cells conferring protection and recognize C. albicans mainly via complement receptor 3. They possess a range of effector mechanisms, contributing to elimination of the pathogen. Neutrophil activation is closely linked to complement and modulated by activated mononuclear cells. A thorough understanding of these mechanisms will help in creating an individualized approach to patients suffering from systemic candidiasis and aid in optimizing clinical management. © 2015 The Author(s). Published with license by Taylor & Francis Group, LLC. Source

Costa A.C.B.P.,Sao Paulo State University | Costa A.C.B.P.,Hans Knoell institute | Pereira C.A.,Sao Paulo State University | Junqueira J.C.,Sao Paulo State University | Jorge A.O.C.,Sao Paulo State University
Virulence | Year: 2013

The Candida genus expresses virulence factors that, when combined with immunosuppression and other risk factors, can cause different manifestations of oral candidiasis. The treatment of mucosal infections caused by Candida and the elucidation of the disease process have proven challenging. Therefore, the study of experimentally induced oral candidiasis in rats and mice is useful to clarify the etiopathology of this condition, improve diagnosis, and search for new therapeutic options because the disease process in these animals is similar to that of human candidiasis lesions. Here, we describe and discuss new studies involving rat and mouse models of oral candidiasis with respect to methods for inducing experimental infection, methods for evaluating the development of experimental candidiasis, and new treatment strategies for oral candidiasis. © 2013 Landes Bioscience. Source

Mehta G.,Aurora University | Ferreira V.P.,University of Toledo | Skerka C.,Hans Knoell institute | Zipfel P.F.,Hans Knoell institute | And 2 more authors.
Molecular Immunology | Year: 2014

Complement factor H (CFH) protein is an inhibitor of the alternative pathway of complement (AP) both in the fluid phase and on the surface of host cells. Mouse and human complement factor H-related (CFHR) proteins also belong to the fH family of plasma glycoproteins. The main goal of the current study was to compare the presence of mRNA for two mCFHR proteins in spontaneously developing autoimmune diseases in mice such as dense deposit disease (DDD), diabetes mellitus (DM), basal laminar deposits (BLD), collagen antibody-induced arthrits (CAIA) and systemic lupus erythematosus (SLE). Here we report for the first time that the CFHR-C mRNA was universally absent in the liver from three strains of lupus-prone mice and in a diabetic-prone mouse strain. The mRNA levels (pg/ng) for CFH and CFHR-B in MRL. -lpr/lpr, at 9. wks and 23. wks were 707.2. ±. 44.4, 54.5. ±. 5.75 and 729. ±. 252.9, 74.04. ±. 22.76, respectively. The mRNA levels for CFH and CFHR-B in NZB/NZW mice, at 9. wks and 54. wks were 579.9. ±. 23.8, 58.8. ±. 1.41 and 890.3. ±. 135.2, 63.30. ±. 9.2, respectively. CFHR-C protein was absent in the circulation of MRL. -lpr/lpr and NZB/NZW mice before and after the development of lupus. Similarly, mRNA and protein for CFHR-C was universally absent in liver and other organs and in the circulation of NOD mice before and after the development of DM. In contrast, the mRNAs for CFH, CFHR-B and CFHR-C were universally present in the liver from mice with and without DDD, BLD and CAIA. The levels of mRNA for CFHR-B in mice with and without BLD were ~4 times higher than the mice with lupus. The complete absence of mRNA for CFHR-C in lupus and diabetic-prone strains indicates that polymorphic variation within the mouse CFHR family exists and raises the possibility that such variation contributes to lupus and diabetic phenotypes. © 2014 Elsevier Ltd. Source

Mayer F.L.,Hans Knoell institute | Wilson D.,Hans Knoell institute | Hube B.,Hans Knoell institute | Hube B.,Universitatsklinikum | Hube B.,Friedrich - Schiller University of Jena
PLoS ONE | Year: 2013

Systemic infections of humans with the fungal pathogen Candida albicans are associated with a high mortality rate. Currently, efficient treatment of these infections is hampered by the relatively low number of available antifungal drugs. We recently identified the small heat shock protein Hsp21 in C. albicans and demonstrated its fundamental role for environmental stress adaptation and fungal virulence. Hsp21 was found in several pathogenic Candida species but not in humans. This prompted us to investigate the effects of a broad range of different antifungal drugs on an Hsp21-null C. albicans mutant strain. Our results indicate that combinatorial therapy targeting Hsp21, together with specific antifungal drug targets, has strong synergistic potential. In addition, we demonstrate that Hsp21 is required for tolerance to ethanol-induced stress and induction of filamentation in response to pharmacological inhibition of Hsp90. These findings might pave the way for the development of new treatment strategies against Candida infections. © 2013 Mayer et al. Source

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